Comparative Resistance ofPhaseolus vulgarisCultivars to Clover Yellow Vein Virus Using Various Inoculation Methods

Plant Disease ◽  
1984 ◽  
Vol 68 (7) ◽  
pp. 555
Author(s):  
V. C. Dwadash-Shreni
Keyword(s):  
Yellow Vein ◽  
Inoculation Methods ◽  
Clover Yellow Vein Virus

scholarly journals The central and C-terminal domains of VPg of Clover yellow vein virus are important for VPg–HCPro and VPg–VPg interactions

2003 ◽  
Vol 84 (10) ◽  
pp. 2861-2869 ◽  
Author(s):  
Ma. Leonora M. Yambao ◽  
Chikara Masuta ◽  
Kenji Nakahara ◽  
Ichiro Uyeda
Keyword(s):  
Amino Acids ◽  
Western Blot ◽  
Yellow Vein ◽  
Transcription Activator ◽  
Yeast Two Hybrid ◽  
Yeast Two Hybrid System ◽  
Clover Yellow Vein Virus ◽  
Two Hybrid ◽  
Far Western Blot

Interactions between the major proteins of Clover yellow vein virus (ClYVV) were investigated using a GAL4 transcription activator-based yeast two-hybrid system (YTHS). Self-interactions manifested by VPg and HCPro and an interaction between NIb and NIaPro were observed in ClYVV. In addition, a strong HCPro–VPg interaction was detected by both YTHS and by in vitro far-Western blot analysis in ClYVV. A potyvirus HCPro–VPg interaction has not been reported previously. Using YTHS, domains in ClYVV for the VPg self-interaction and the HCPro–VPg interaction were mapped. The VPg C-terminal region (38 amino acids) was important for the VPg–VPg interaction and the central 19 amino acids were needed for the HCPro–VPg interaction.

scholarly journals P3N-PIPO, a Frameshift Product from theP3Gene, Pleiotropically Determines the Virulence of Clover Yellow Vein Virus in both Resistant and Susceptible Peas

2016 ◽  
Vol 90 (16) ◽  
pp. 7388-7404 ◽  
Author(s):  
Go Atsumi ◽  
Haruka Suzuki ◽  
Yuri Miyashita ◽  
Sun Hee Choi ◽  
Yusuke Hisa ◽  
...  
Keyword(s):  
Cell Death ◽  
Resistance Gene ◽  
Systemic Infection ◽  
Viral Disease ◽  
Hypersensitive Reaction ◽  
Yellow Vein ◽  
Recessive Resistance ◽  
Content Type ◽  
Clover Yellow Vein Virus ◽  
And Control

ABSTRACTPeas carrying thecyv1recessive resistance gene are resistant to clover yellow vein virus (ClYVV) isolates No.30 (Cl-No.30) and 90-1 (Cl-90-1) but can be infected by a derivative of Cl-90-1 (Cl-90-1 Br2). The main determinant for the breaking ofcyv1resistance by Cl-90-1 Br2 is P3N-PIPO produced from theP3gene via transcriptional slippage, and the higher level of P3N-PIPO produced by Cl-90-1 Br2 than by Cl-No.30 contributes to the breaking of resistance. Here we show that P3N-PIPO is also a major virulence determinant in susceptible peas that possess another resistance gene,Cyn1, which does not inhibit systemic infection with ClYVV but causes hypersensitive reaction-like lethal systemic cell death. We previously assumed that the susceptible pea cultivar PI 226564 has a weak allele ofCyn1. Cl-No.30 did not induce cell death, but Cl-90-1 Br2 killed the plants. Our results suggest that P3N-PIPO is recognized byCyn1and induces cell death. Unexpectedly, heterologously strongly expressed P3N-PIPO of Cl-No.30 appears to be recognized byCyn1in PI 226564. The level of P3N-PIPO accumulation from theP3gene of Cl-No.30 was significantly lower than that of Cl-90-1 Br2 in aNicotiana benthamianatransient assay. Therefore,Cyn1-mediated cell death also appears to be determined by the level of P3N-PIPO. The more efficiently a ClYVV isolate brokecyv1resistance, the more it induced cell death systemically (resulting in a loss of the environment for virus accumulation) in susceptible peas carryingCyn1, suggesting that antagonistic pleiotropy of P3N-PIPO controls the resistance breaking of ClYVV.IMPORTANCEControl of plant viral disease has relied on the use of resistant cultivars; however, emerging mutant viruses have broken many types of resistance. Recently, we revealed that Cl-90-1 Br2 breaks the recessive resistance conferred bycyv1, mainly by accumulating a higher level of P3N-PIPO than that of the nonbreaking isolate Cl-No.30. Here we show that a susceptible pea line recognized the increased amount of P3N-PIPO produced by Cl-90-1 Br2 and activated the salicylic acid-mediated defense pathway, inducing lethal systemic cell death. We found a gradation of virulence among ClYVV isolates in acyv1-carrying pea line and two susceptible pea lines. This study suggests a trade-off between breaking of recessive resistance (cyv1) and host viability; the latter is presumably regulated by the dominantCyn1gene, which may impose evolutionary constraints uponP3N-PIPOfor overcoming resistance. We propose a working model of the host strategy to sustain the durability of resistance and control fast-evolving viruses.

scholarly journals Characterization and Nucleotide Sequence of the 3' Terminal Region of Clover Yellow Vein Virus Isolated from Gentian (Gentiana spp.).

1997 ◽  
Vol 63 (4) ◽  
pp. 328-333 ◽  
Author(s):  
Takahide SASAYA ◽  
Kazuhiko KAJI ◽  
Ichiro FUJISAWA ◽  
Hiroki KOGANEZAWA ◽  
Takeshi TERAOKA ◽  
...  
Keyword(s):  
Nucleotide Sequence ◽  
Terminal Region ◽  
Yellow Vein ◽  
Clover Yellow Vein Virus
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